Human Coronavirus 229E Binds to CD13 in Rafts and Enters the Cell through Caveolae

• Ryuji Nomura

  Department of Anatomy I, Fujita Health University School of Medicine, Toyoake 470-1192

• Asuka Kiyota

  Department of Histology and Cell Biology, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8551

• Etsuko Suzaki

  Department of Histology and Cell Biology, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8551

• Katsuko Kataoka

  Department of Histology and Cell Biology, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8551

• Yoshihide Ohe

  Biosignal Research Center, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi 371-8512

• Kaoru Miyamoto

  Department of Biochemistry, Fukui Medical University, Matsuoka 910-1193

• Takao Senda

  Department of Anatomy I, Fujita Health University School of Medicine, Toyoake 470-1192

• Toyoshi Fujimoto

  Department of Anatomy and Molecular Cell Biology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan

抄録

CD13, a receptor for human coronavirus 229E (HCoV-229E), was identified as a major component of the Triton X-100-resistant membrane microdomain in human fibroblasts. The incubation of living fibroblasts with an anti-CD13 antibody on ice gave punctate labeling that was evenly distributed on the cell surface, but raising the temperature to 37°C before fixation caused aggregation of the labeling. The aggregated labeling of CD13 colocalized with caveolin-1 in most cells. The HCoV-229E virus particle showed a binding and redistribution pattern that was similar to that caused by the anti-CD13 antibody: the virus bound to the cell evenly when incubated on ice but became colocalized with caveolin-1 at 37°C; importantly, the virus also caused sequestration of CD13 to the caveolin-1-positive area. Electron microscopy confirmed that HCoV-229E was localized near or at the orifice of caveolae after incubation at 37°C. The depletion of plasmalemmal cholesterol with methyl β-cyclodextrin significantly reduced the HCoV-229E redistribution and subsequent infection. A caveolin-1 knockdown by RNA interference also reduced the HCoV-229E infection considerably. The results indicate that HCoV-229E first binds to CD13 in the Triton X-100-resistant microdomain, then clusters CD13 by cross-linking, and thereby reaches the caveolar region before entering cells.

収録刊行物

• Journal of Virology

  Journal of Virology 78 (16), 8701-8708, 2004-08-15

  American Society for Microbiology

キーワード

• Virology
• Insect Science
• Immunology
• Microbiology

詳細情報

• CRID: 1363107370897740032
• NII論文ID: 30020800294
• DOI: 10.1128/jvi.78.16.8701-8708.2004
• ISSN: 10985514
• ISSN: 0022538X
• Web Site: https://journals.asm.org/doi/pdf/10.1128/JVI.78.16.8701-8708.2004
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